CNS sensory and motor (Lecture 6).pdf

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School

McGill University

Department

Physiology

Course

PHGY 209

Professor

Erik Cook

Semester

Fall

Description

CNS sensory and motor (Lecture 6):
Color blindness:
 Genetic defect in the opsins: one of the opsins is not functioning.
o You may have just two types of cones or maybe just one,
which limits the range of colours we can perceive.
 Fairly common, mostly in men.
Flow of visual information in the brain:
 We will now look at some of the pathways that go from the retina to the brain.
 This is the brain turned upside down. In the middle, we see the brainstem.
 Right and left visual field: opposite, because the subject has been turned over.
 Each eye sees the entire visual field, but we can split each visual field into green, on one
side, and blue, on the other side. The blues are on the same side, on the right visual field,
the green, on the left visual field.
 Because the optics of the eyes functions like a camera, the image is inverted when it is
projected on the retina in the back. Now the blue right visual field is on the left, and the
green visual field is also on the side.
 In the somatosensory system eventually everything gets put on the contralateral side of
the CNS.
 Recall: the dorsal columns cross in the medulla. Where do the anterolateral columns
cross? Trick question, since they’ve already crossed by the time they form the
anterolateral columns. Pain and temperature, touch and proprioception are all going to get
to the contralateral side of the brain.
 The somatosensory cortex in the post-central gyrus, right behind the central sulcus, is a
contralateral representation of our body.
 The visual system also has a contralateral representation, but more complicated.
o Both eyes see both visual fields. So, leaving the eye are the axons of the ganglion
cells, which is called the optic nerve. This contains the image from both visual
fields (both sides -> blue and green axons).
o Something interesting happens at the base of the brain: optic chiasm. There is a
switch, but not all fibers switch sides, only some do.
o Which fibers switch side? The NASAL fibers that are originating from the retina
closest to the nose (aka nasal portion of the retina) cross. The temporal portion of
the retina closest to the temporal lobes do not cross.
o After the optic chiasm, we have the optic tract, composed of information from
both eyes and only the contralateral visual field due to the crossing of nasal fibers.
o This contralateral representation of the visual world is then carried to the lateral
geniculate nucleus (Thalamus), a relay station.
o Projections: optic radiations that swing up and end up at the very back of the
brain, in the occipital lobe called the visual cortex => primary visual cortex, first
cortical stage of the visual processing.
 This cortex carries information from both eyes in the form of a
contralateral representation.  Eventually, the two separate sides of visual information get put together, as
we move forward from the visual cortex. We will talk about what happens
next after the primary visual cortex.
 This anatomical crossing representation has some interesting effects, when we talk about
lesions.
The anatomy of visual field deficits
Structure/function relationships:
1. A patient who cannot see from one of his eyes: the lesion has to be either in the retina or
in the optic nerve. This is the only place that you can damage and eliminate vision in only
one eye, since the optic nerve carries the R and L visual fields from a single eye.
2. When we cut the optic tract anywhere after the optic chiasm, the deficit is a contralateral
loss of vision in both eyes, never ipsilateral when beyond OC.
3. Cut in the optic chiasm down the midline, we are cutting the axons that are crossing,
which are coming from the nasal portion of the retina, so they will only see the temporal
visual field, since things are inverted in the eye. So if we cut only the nasal fibers, we get
a bilateral loss of temporal visual hemifields. (Remark: The nasal portion of the retina
sees the temporal portion of the visual fields, since eyes invert everything).
4. Any lesion beyond the optic chiasm up to the visual cortex causes loss of vision in the
contralateral visual fields, just like in the somatosensory cortex.
o Q/A - Note: If you were to lesion only a small part of the visual cortex, you would
have a contralateral loss of vision in a small part of the visual field. Small lesions
produce small deficits. So, in part 4, we are talking about the lesion of the entire
projections.
o These lesions are tricky since both eyes see both visual fields. Cortical representation of the visual world:
 We don’t know enough from this course to talk in depth about what happens next.
 There are parts of the brain that don’t respond to center surround receptor field structures.
 How do RFs respond to faces, hands and complicated images? It all starts in the primary
visual cortex. It turns out that the RFs structure of RGM looks a lot like the ganglion
cells: center surround RFs structures. When we get to the visual cortex, listen to these
neurons and find out what kind of pattern they like in their receptor field (i.e. that part of
the visual world the neuron responds to) and what causes the cortical neurons to respond
best are not donut shaped patterns of light (like the ganglion cells), but elongated line
segments oriented in the right orientations: some like vertical, horizontal, some like 45
degrees. What happens is that we are extracting these features, and then as we move
through other visual areas in the cortex, about half of which has neurons that respond to
visual stimuli, the type of receptor fields we form in these neurons get larger, so that
these neurons start responding to more complex features.
 There are two major streams of visual information:
o Parietal visual stream (going up from the primary visual cortex to the parietal
lobe, commonly called the Where pathway since it responds to very precisely to
locations, spatial features and motion -> helps you figure out spatially where
things are). Polymodal (visual info gets mixed with other modalities like
somatosensory to start bringing in where your external environment is positioned,
where objects are located, what’s moving,
etc. -> top part of the where pathway).
o Temporal visual stream (What pathway): As
you go through this stream, you find neurons
whose RFs get bigger and start responding to
complex image features (faces & hands).
 Recall: the motion-processing area of the brain right
around the top of the green area.
 So, we started from the retina, it sends center
surround RF structures (donut-shaped), gets to the
primary visual cortex (where the donut shapes are turned now into line segments/edges and then transformed into motion, location or into
complex visual features).
 What we think of a model that goes from center surround to oriented line segments? Min.
37-38:53 (not on the test).
Sensory modalities:
 We will now talk about the auditory system due to mechanoreceptors.
Amplitude and frequency of sound:
 Sound are pressure waves where molecules of the air become closer together (dark
circles) followed by, a few miliseconds later, a little farther apart (white circles). Closer-
farther-closer-farther,etc.
 Pressure travels past our head and this is the energy that we use to detect for sound.
 We can decompose sound into its frequency or pitch (music term) – nb of pressure waves
per second flying past our head, measured in Hertz.
 Amplitude: loudness of the sound, from where the molecules are packed together to
where they’re farther apart. Normal audibility curve:
 What is the relationship between the amplitude of the sound and what we hear?
 First, we don’t hear different frequencies the same way?
 Bottom line is the threshold: m